RapamycinFungusV1, Main, Exploration, bibRecord, 000938

A pathway of targeted autophagy is induced by DNA damage in budding yeast.

Identifieur interne : 000938 ( Main/Exploration ); précédent : 000937; suivant : 000939

A pathway of targeted autophagy is induced by DNA damage in budding yeast.

Auteurs : Vinay V. Eapen [États-Unis] ; David P. Waterman [États-Unis] ; Amélie Bernard [États-Unis] ; Nathan Schiffmann ; Enrich Sayas [Suisse] ; Roarke Kamber [États-Unis] ; Brenda Lemos [États-Unis] ; Gonen Memisoglu [États-Unis] ; Jessie Ang [États-Unis] ; Allison Mazella [États-Unis] ; Silvia G. Chuartzman ; Robbie J. Loewith [Suisse] ; Maya Schuldiner ; Vladimir Denic [États-Unis] ; Daniel J. Klionsky [États-Unis] ; James E. Haber [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2017.

RBID : pubmed:28154131

Descripteurs français

English descriptors

Abstract

Autophagy plays a central role in the DNA damage response (DDR) by controlling the levels of various DNA repair and checkpoint proteins; however, how the DDR communicates with the autophagy pathway remains unknown. Using budding yeast, we demonstrate that global genotoxic damage or even a single unrepaired double-strand break (DSB) initiates a previously undescribed and selective pathway of autophagy that we term genotoxin-induced targeted autophagy (GTA). GTA requires the action primarily of Mec1/ATR and Rad53/CHEK2 checkpoint kinases, in part via transcriptional up-regulation of central autophagy proteins. GTA is distinct from starvation-induced autophagy. GTA requires Atg11, a central component of the selective autophagy machinery, but is different from previously described autophagy pathways. By screening a collection of ∼6,000 yeast mutants, we identified genes that control GTA but do not significantly affect rapamycin-induced autophagy. Overall, our findings establish a pathway of autophagy specific to the DNA damage response.

DOI: 10.1073/pnas.1614364114
PubMed: 28154131
PubMed Central: PMC5320992

Affiliations:

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Le document en format XML

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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Ang, Jessie" sort="Ang, Jessie" uniqKey="Ang J" first="Jessie" last="Ang">Jessie Ang</name>
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<affiliation wicri:level="4"><nlm:affiliation>Institute of Genetics and Genomics in Geneva, University of Geneva, CH-1211 Geneva 4, Switzerland.</nlm:affiliation>
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<author><name sortKey="Denic, Vladimir" sort="Denic, Vladimir" uniqKey="Denic V" first="Vladimir" last="Denic">Vladimir Denic</name>
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<author><name sortKey="Haber, James E" sort="Haber, James E" uniqKey="Haber J" first="James E" last="Haber">James E. Haber</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (genetics)</term>
<term>Autophagy-Related Proteins (genetics)</term>
<term>Autophagy-Related Proteins (metabolism)</term>
<term>Cell Cycle Proteins (genetics)</term>
<term>Cell Cycle Proteins (metabolism)</term>
<term>Checkpoint Kinase 2 (genetics)</term>
<term>Checkpoint Kinase 2 (metabolism)</term>
<term>DNA Breaks, Double-Stranded (MeSH)</term>
<term>DNA Damage (MeSH)</term>
<term>DNA Repair (MeSH)</term>
<term>DNA, Fungal (genetics)</term>
<term>DNA, Fungal (metabolism)</term>
<term>Intracellular Signaling Peptides and Proteins (genetics)</term>
<term>Intracellular Signaling Peptides and Proteins (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (genetics)</term>
<term>Vesicular Transport Proteins (genetics)</term>
<term>Vesicular Transport Proteins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ADN fongique (génétique)</term>
<term>ADN fongique (métabolisme)</term>
<term>Altération de l'ADN (MeSH)</term>
<term>Autophagie (génétique)</term>
<term>Cassures double-brin de l'ADN (MeSH)</term>
<term>Checkpoint kinase 2 (génétique)</term>
<term>Checkpoint kinase 2 (métabolisme)</term>
<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Protéines associées à l'autophagie (génétique)</term>
<term>Protéines associées à l'autophagie (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines du cycle cellulaire (génétique)</term>
<term>Protéines du cycle cellulaire (métabolisme)</term>
<term>Protéines du transport vésiculaire (génétique)</term>
<term>Protéines du transport vésiculaire (métabolisme)</term>
<term>Protéines et peptides de signalisation intracellulaire (génétique)</term>
<term>Protéines et peptides de signalisation intracellulaire (métabolisme)</term>
<term>Réparation de l'ADN (MeSH)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Transduction du signal (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Proteins</term>
<term>Cell Cycle Proteins</term>
<term>Checkpoint Kinase 2</term>
<term>DNA, Fungal</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Vesicular Transport Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
<term>Saccharomyces cerevisiae</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN fongique</term>
<term>Autophagie</term>
<term>Checkpoint kinase 2</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines associées à l'autophagie</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
<term>Protéines du transport vésiculaire</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Saccharomyces cerevisiae</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autophagy-Related Proteins</term>
<term>Cell Cycle Proteins</term>
<term>Checkpoint Kinase 2</term>
<term>DNA, Fungal</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Vesicular Transport Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ADN fongique</term>
<term>Checkpoint kinase 2</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines associées à l'autophagie</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
<term>Protéines du transport vésiculaire</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>DNA Breaks, Double-Stranded</term>
<term>DNA Damage</term>
<term>DNA Repair</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Altération de l'ADN</term>
<term>Cassures double-brin de l'ADN</term>
<term>Réparation de l'ADN</term>
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<front><div type="abstract" xml:lang="en">Autophagy plays a central role in the DNA damage response (DDR) by controlling the levels of various DNA repair and checkpoint proteins; however, how the DDR communicates with the autophagy pathway remains unknown. Using budding yeast, we demonstrate that global genotoxic damage or even a single unrepaired double-strand break (DSB) initiates a previously undescribed and selective pathway of autophagy that we term genotoxin-induced targeted autophagy (GTA). GTA requires the action primarily of Mec1/ATR and Rad53/CHEK2 checkpoint kinases, in part via transcriptional up-regulation of central autophagy proteins. GTA is distinct from starvation-induced autophagy. GTA requires Atg11, a central component of the selective autophagy machinery, but is different from previously described autophagy pathways. By screening a collection of ∼6,000 yeast mutants, we identified genes that control GTA but do not significantly affect rapamycin-induced autophagy. Overall, our findings establish a pathway of autophagy specific to the DNA damage response.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28154131</PMID>
<DateCompleted><Year>2018</Year>
<Month>04</Month>
<Day>24</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>06</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>114</Volume>
<Issue>7</Issue>
<PubDate><Year>2017</Year>
<Month>02</Month>
<Day>14</Day>
</PubDate>
</JournalIssue>
<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation>
</Journal>
<ArticleTitle>A pathway of targeted autophagy is induced by DNA damage in budding yeast.</ArticleTitle>
<Pagination><MedlinePgn>E1158-E1167</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1614364114</ELocationID>
<Abstract><AbstractText>Autophagy plays a central role in the DNA damage response (DDR) by controlling the levels of various DNA repair and checkpoint proteins; however, how the DDR communicates with the autophagy pathway remains unknown. Using budding yeast, we demonstrate that global genotoxic damage or even a single unrepaired double-strand break (DSB) initiates a previously undescribed and selective pathway of autophagy that we term genotoxin-induced targeted autophagy (GTA). GTA requires the action primarily of Mec1/ATR and Rad53/CHEK2 checkpoint kinases, in part via transcriptional up-regulation of central autophagy proteins. GTA is distinct from starvation-induced autophagy. GTA requires Atg11, a central component of the selective autophagy machinery, but is different from previously described autophagy pathways. By screening a collection of ∼6,000 yeast mutants, we identified genes that control GTA but do not significantly affect rapamycin-induced autophagy. Overall, our findings establish a pathway of autophagy specific to the DNA damage response.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Eapen</LastName>
<ForeName>Vinay V</ForeName>
<Initials>VV</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Waterman</LastName>
<ForeName>David P</ForeName>
<Initials>DP</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bernard</LastName>
<ForeName>Amélie</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schiffmann</LastName>
<ForeName>Nathan</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Genetics, Weizmann Institute of Sciences, Rehovot, Israel 7610001.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sayas</LastName>
<ForeName>Enrich</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Genetics and Genomics in Geneva, University of Geneva, CH-1211 Geneva 4, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kamber</LastName>
<ForeName>Roarke</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Molecular and Cell Biology, Harvard University, Cambridge, MA 02138.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lemos</LastName>
<ForeName>Brenda</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Memisoglu</LastName>
<ForeName>Gonen</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ang</LastName>
<ForeName>Jessie</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mazella</LastName>
<ForeName>Allison</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chuartzman</LastName>
<ForeName>Silvia G</ForeName>
<Initials>SG</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Genetics, Weizmann Institute of Sciences, Rehovot, Israel 7610001.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Loewith</LastName>
<ForeName>Robbie J</ForeName>
<Initials>RJ</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Genetics and Genomics in Geneva, University of Geneva, CH-1211 Geneva 4, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schuldiner</LastName>
<ForeName>Maya</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Genetics, Weizmann Institute of Sciences, Rehovot, Israel 7610001.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Denic</LastName>
<ForeName>Vladimir</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Molecular and Cell Biology, Harvard University, Cambridge, MA 02138.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Klionsky</LastName>
<ForeName>Daniel J</ForeName>
<Initials>DJ</Initials>
<AffiliationInfo><Affiliation>Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Haber</LastName>
<ForeName>James E</ForeName>
<Initials>JE</Initials>
<AffiliationInfo><Affiliation>Department of Biology, Brandeis University, Waltham, MA 02454; haber@brandeis.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 GM053396</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM121419</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM061766</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R37 GM020056</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM020056</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 GM007122</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
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<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>02</Month>
<Day>02</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Proc Natl Acad Sci U S A</MedlineTA>
<NlmUniqueID>7505876</NlmUniqueID>
<ISSNLinking>0027-8424</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C502923">Atg11 protein, S cerevisiae</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071183">Autophagy-Related Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018797">Cell Cycle Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004271">DNA, Fungal</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance>
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<NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D033921">Vesicular Transport Proteins</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.11</RegistryNumber>
<NameOfSubstance UI="D064447">Checkpoint Kinase 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="C088937">MEC1 protein, S cerevisiae</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.12.1</RegistryNumber>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071183" MajorTopicYN="N">Autophagy-Related Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018797" MajorTopicYN="N">Cell Cycle Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064447" MajorTopicYN="N">Checkpoint Kinase 2</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053903" MajorTopicYN="Y">DNA Breaks, Double-Stranded</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004249" MajorTopicYN="Y">DNA Damage</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004260" MajorTopicYN="N">DNA Repair</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004271" MajorTopicYN="N">DNA, Fungal</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047908" MajorTopicYN="N">Intracellular Signaling Peptides and Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D033921" MajorTopicYN="N">Vesicular Transport Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ATM kinase</Keyword>
<Keyword MajorTopicYN="Y">ATR kinase</Keyword>
<Keyword MajorTopicYN="Y">DNA damage</Keyword>
<Keyword MajorTopicYN="Y">autophagy</Keyword>
<Keyword MajorTopicYN="Y">budding yeast</Keyword>
</KeywordList>
</MedlineCitation>
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<Day>6</Day>
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A pathway of targeted autophagy is induced by DNA damage in budding yeast.

A pathway of targeted autophagy is induced by DNA damage in budding yeast.

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